Abstract
Background: Opening of the cyclosporin A (CsA)-sensitive mitochondrial transition pore (MTP) is induced by thyroid hormone treatment. Objective: To evaluate the role played by MTP in ischemia-reperfusion damage in hyperthyroid hearts. Animals and methods: Rats were injected with 200 μg/kg 3,3',5-triiodo-L-thyronine for six days. Hyperthyroid and non-treated hearts perfused in the Langendorff model were subjected to 30 min of no flow global ischemia followed by 30 min of reperfusion. CsA was added during preischemic perfusion and throughout the reperfusion period. Results: Hyperthyroidism enhanced the initiation and completion of ischemic contracture. CsA had no effect on ischemic parameters, indicating that MTP was not involved in ischemic contracture. Recovery of contractile performance in reperfused hyperthyroid hearts was delayed compared with euthyroid hearts. CsA significantly enhanced the recovery of contractile performance, oxygen consumption, and ATP and phosphocreatine content in reperfused hyperthyroid hearts. Conclusions: Induction of MTP opening by thyroid hormone treatment aggravates ischemia-reperfusion damage in the reperfused hyperthyroid heart. Preventing MTP opening by CsA results in unmasking beneficial metabolic and hemodynamic effects of thyroid hormone.
| Original language | English |
|---|---|
| Pages (from-to) | 77-81 |
| Number of pages | 5 |
| Journal | Experimental and Clinical Cardiology |
| Volume | 5 |
| Issue number | 2 |
| State | Published - 2000 |
| Externally published | Yes |
Keywords
- Energy metabolism
- Hormones
- Ischemia
- Mitochondria
- Reperfusion